Reitz B A, Prager D J, Feigen G A
J Exp Med. 1968 Dec 1;128(6):1401-24. doi: 10.1084/jem.128.6.1401.
The response of isolated guinea pig hearts to perfusion with purified streptolysin O is characterized by a rapid, but transient, decrease in rate and amplitude of contraction; these reactions are superimposed upon a gradual, irreversible, loss of ventricular contractility. At ventricular standstill, the atria continue to beat spontaneously in a normal way. Isolated ventricle strips prepared from such preparations can be driven electrically, and their behavior is functionally indistinguishable from that of similar preparations made from normal hearts. Tests on spontaneously beating isolated atrial pairs show that the toxin induces a dose-dependent, reversible, decline in rate and amplitude which is accompanied by a marked, but transient, increase in the velocity of repolarization of the intracellular potential. The atrial reactions were completely blocked by atropine and potentiated by eserine. Acetylcholine was detected in the perfusates obtained by incubating a large pool of atrial tissue with active toxin, supporting the inference that the transient mechanical and electrophysiological reactions to toxin might be consequences of the release of acetylcholine from these tissues by the active toxin. Control studies showed that only the active toxin had the capacity to induce the cardiac responses. The toxin was active only in the reduced but not the oxidized form. The effects of the active toxin were modified if it were heated prior to challenge, and they could be neutralized by specific antiserum and inhibited by cholesterol. Since the driven ventricle strip was mechanically and electrophysiologically insensitive to streptolysin O, the irreversible changes in the whole heart must have occurred because of a defect in the atrioventricular conduction system.
离体豚鼠心脏对纯化的链球菌溶血素O灌注的反应特点是，收缩速率和幅度迅速但短暂地降低；这些反应叠加在心室收缩力逐渐、不可逆的丧失之上。在心室停搏时，心房仍以正常方式自发搏动。从这类标本制备的离体心室条带可被电驱动，其行为在功能上与从正常心脏制备的类似标本无异。对自发搏动的离体心房对进行的测试表明，该毒素诱导速率和幅度呈剂量依赖性、可逆性下降，同时伴有细胞内电位复极化速度明显但短暂的增加。心房反应完全被阿托品阻断，被毒扁豆碱增强。在用活性毒素孵育大量心房组织获得的灌注液中检测到了乙酰胆碱，这支持了以下推断：对毒素的短暂机械和电生理反应可能是活性毒素使这些组织释放乙酰胆碱的结果。对照研究表明，只有活性毒素有能力诱导心脏反应。该毒素仅在还原形式而非氧化形式下具有活性。如果在激发前加热活性毒素，其作用会改变，并且可被特异性抗血清中和，被胆固醇抑制。由于被驱动的心室条带对链球菌溶血素O在机械和电生理上不敏感，整个心脏的不可逆变化一定是由于房室传导系统的缺陷所致。
